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Impaired memory is more closely associated with brain beta-amyloid than leukoaraiosis in hypertensive patients with
Eric E Smith1,2, Alona Muzikansky3, Cheryl R McCreary4
1Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.
Insights
Hypertension is linked to cognitive decline. Alzheimer's pathology, detected by PiB-PET, significantly impacts episodic memory in hypertensive individuals, even without dementia.
Area of Science:
- Neuroscience
- Gerontology
- Cardiology
Background:
- Hypertension is a major modifiable risk factor for subcortical ischemic changes and Alzheimer's dementia.
- Investigating the pathological basis of early cognitive symptoms in hypertensive patients is crucial.
Purpose of the Study:
- To use neuroimaging to explore the pathological underpinnings of early cognitive symptoms in hypertensive individuals.
- To correlate neuroimaging findings with cognitive test performance in this population.
Main Methods:
- A cross-sectional cohort study included 67 hypertensive patients (age >60) without dementia but with mild cognitive impairment or subjective cognitive concerns.
- Magnetic Resonance Imaging (MRI) assessed subcortical vascular changes.
- Positron Emission Tomography (PET) with Pittsburgh Compound B (PiB-PET) measured beta-amyloid deposition.
Main Results:
- Episodic memory was significantly impaired (mean Z score -0.63).
- Increased cortical PiB-PET binding was associated with lower episodic memory scores (0.14 SD lower per 0.1 unit increase).
- Vascular markers (white matter hyperintensities, silent infarcts, microbleeds) did not correlate with cognitive scores.
Conclusions:
- Episodic memory deficits in hypertensive individuals with cognitive concerns are linked to Alzheimer's pathology (beta-amyloid deposition).
- This suggests a significant role of Alzheimer's pathology in cognitive impairment, even in those at high risk for vascular cognitive impairment.
Background:
Hypertension is the strongest modifiable risk factor for subcortical ischemic changes and is also a risk factor for Alzheimer's dementia. We used neuroimaging to investigate the pathological basis of early cognitive symptoms in patients with hypertension.
Methods:
In this cross-sectional cohort study 67 patients age >60 years with hypertension and Clinical Dementia Rating scale score of 0.5 without dementia, and without history of symptomatic stroke, underwent MRI for measurement of subcortical vascular changes and positron emission tomography (PET) scan with Pittsburgh Compound B (PiB-PET) to detect beta-amyloid deposition. These imaging measures were related to neuropsychological tests of memory, executive function and processing speed.
Results:
Mean age was 75.0 (standard deviation, SD, 7.3). Mean neuropsychological Z scores were: episodic memory -0.63 (SD 1.23), executive function -0.40 (SD 1.10), processing speed -0.24 (SD 0.88); 22 of the 67 subjects met criteria for mild cognitive impairment (MCI) and the remaining 45 subjects had subjective cognitive concerns only. In multivariable models adjusting for age and years of education, each 0.1 unit increase in mean cortical PiB-PET binding was associated with 0.14 lower mean Z score for episodic memory (95% CI -0.28 to -0.01). This means that for every 0.1 unit increase in mean cortical PiB-PET, episodic memory was 0.14 standard deviations lower. White matter hyperintensity volume, silent brain infarcts and microbleeds were not associated with neuropsychological test scores.
Conclusions:
Episodic memory was prominently affected in hypertensive participants with MCI or subjective cognitive concerns, and was associated with PiB-PET binding. This suggests a prominent role for Alzheimer pathology in cognitive impairment even in hypertensive participants at elevated risk for vascular cognitive impairment.
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